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Growth-inhibitory effect of tamoxifen and quercetin and presence of type II estrogen binding sites in human laryngeal cancer cell lines and primary laryngeal tumors by Gabriella Ferrandina; Giovanni Almadori; Nicola Maggiano; Paola Lanza; Cristiano Ferlini; Paola Cattani; Mauro Piantelli; Giovanni Scambia; Franco O. Ranelletti is a Medicine article available to read on EtoBox.

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Quercetin and tamoxifen, in a range of concentrations between 0.01 and 5 M, exert a dose-dependent inhibition on the anchorage-dependent and anchorage-independent cell growth of Hep2 and CO-K3 laryngeal cancer cell lines. Cell cycle analysis revealed that the growth-inhibitory effect was associated with a block of the cells at the G 2 /M checkpoint of the cell cycle followed by DNA fragmentation. This suggests that the failure of cells to proceed through the G 2 /M checkpoint can be a trigger for apoptosis. The induction of apoptosis by quercetin and tamoxifen was confirmed immunocytochemically by the in situ nick end labeling (TUNEL) reaction. ## These compounds also exerted a dose-dependent growthinhibitory effect on primary tumor cells, as assessed by colony-forming assay and bromodeoxyuridine labeling. Laryngeal cancer cell lines and primary tumor cells expressed Type II estrogen binding sites (Type II EBS) with binding characteristics similar to those of Type II EBS in other tumor cells. Since the affinities of quercetin and tamoxifen for Type II EBS were correlated with their growth-inhibitory potential while ipriflavone neither interacted with these sites nor inhibited cell

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Author

Gabriella Ferrandina; Giovanni Almadori; Nicola Maggiano; Paola Lanza; Cristiano Ferlini; Paola Cattani; Mauro Piantelli; Giovanni Scambia; Franco O. Ranelletti

Publisher

John Wiley and Sons; Wiley (John Wiley & Sons); John Wiley & Sons Inc.; Wiley; Research Square; Test accounts (ISSN 0020-7136)

Published

1998

Language

EN

Field

Medicine (Health Sciences)